There is a long-standing observation in pediatric surgery that a neonate seldom demonstrates wound healing problems. Adult healing occurs by an orchestrated sequence of events in which both new cellular population and new matrix deposition replace a defect, an imperfect process exemplified by the inability to regain the full tensile strength of normal dermis. An open full-thickness soft tissue defect is repaired through the process of wound contraction, in which fibroblasts interact with collagen fibrils producing contractile forces. In contrast to wound contraction is the complication of scar contracture, whereby the process of contraction occurs in healed epithelialized wounds and results in decreased mechanical function. At a molecular level, the interaction of actin- myosin filaments in the microfilaments of fibroblasts has been shown to be the "engine" that drives the contractile process. Actin-myosin interaction depends on the phosphorylation of the myosin light chains at the terminal end of the myosin molecule. Phosphorylation of myosin light chains (LC20) by myosin light chain kinase (MLCK) is required for activation of cell microfilament contraction. The activity of MLCK controls the contraction of microfilaments. Through the study of the molecular interactions of fetal and adult fibroblasts, this project's specific aim is to demonstrate that the amount of myosin ATPase activity is directly proportional to the degree of wound contraction. The long- term goals parallel the clinical implications of this project. The ability to control the amount of contraction in an open defect wound improve current management of large open wounds and burns.